Central Gain Model for Tinnitus: A Review on Noise-Induced Plasticity or When Less at the Periphery Is More in the Center

Hearing loss represents a major sensory deficit as it is largely prevalent in the general population and can dramatically impair quality of life. One of the most prevalent causes of sensorineural hearing loss is noise exposure. Noise-induced hearing loss (NIHL) is the second most common form of the sensorineural hearing deficit, after age-related hearing loss. Importantly, it induces neuropathophysiological alterations in the auditory system, which can result in the generation of “aberrant auditory perceptions” such as tinnitus or hyperacusis. Here, we review the central plasticity that is triggered by noise-induced hearing loss. In brief, there is overwhelming evidence that noise-induced hearing loss is associated to compensatory mechanisms in the auditory centers: while the sensory inputs are reduced at the periphery (i.e., in the cochlear nerve), they are enhanced at virtually all levels of the auditory centers. A vast repertoire of molecular mechanisms are involved in these functional changes. It is plausible that these peripherally triggered central changes can result in tinnitus and/or hyperacusis.